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PubMed2000

Isolation and characterization of porcine circovirus type 2 from pigs showing signs of post-weaning multisystemic wasting syndrome in The Netherlands.

Pigs with wasting syndrome were examined for macroscopic and histopathological lesions, and for porcine circovirus (PCV). Histopathological lesions were comparable to those previously documented for post-weaning multisystemic wasting syndrome (PMWS). In addition, in seven out of ten examined PMWS-affected pigs focal-to-slight mononuclear meningitis and focal cerebral mononuclear infiltrates (4 out of 10) were observed. A virus was isolated from organs and sera from pigs showing wasting syndrome. An immunoperoxidase monolayer assay and an indirect immunofluorescence assay were performed on the infected PK-15 and Dulac cell cultures, respectively, and both assays indicated the presence of PCV type 2 (PCV2). The nested-polymerase chain reaction (nPCR) technique, based on the use of PCV2 specific oligonucleotides, revealed specific amplified products of 481 bp. Nucleotide sequence analysis of the entire genome of the Dutch PCV isolate 24657 NL showed a homology with known nucleotide sequences of porcine PCV type 1 (PCV1) and PCV2 isolates of 77.1% and >96%, respectively. This is the first report of the isolation and characterization of PCV2 in PMWS-affected pigs in the Netherlands.

Animals↗

PubMed1999

Lack of evidence of conserved lentiviral sequences in pigs with post weaning multisystemic wasting syndrome.

In order to investigate the role of retroviruses in the recently described porcine postweaning multisystemic wasting syndrome (PMWS) serum and leukocytes were screened for reverse transcriptase (RT) activity, and tissues were examined for the presence of conserved lentiviral sequences using degenerate primers in a polymerase chain reaction (PCR). Serum and stimulated leukocytes from the blood and lymph nodes from pigs with PMWS, as well as from control pigs had RT activity that was detected by the sensitive Amp-RT assay. A 257-bp fragment was amplified from DNA from the blood and bone marrow of pigs with PMWS. This fragment was identical in size to conserved lentiviral sequences that were amplified from plasmids containing DNA from several lentiviruses. Cloning and sequencing of the fragment from affected pigs, however, did not reveal homology with the recognized lentiviruses. Together the results of these analyses suggest that the RT activity present in tissues from control and affected pigs is the result of endogenous retrovirus expression, and that a lentivirus is not a primary pathogen in PMWS.

Amino Acid Sequence↗

PubMed2000

Viral wasting syndrome of swine: experimental reproduction of postweaning multisystemic wasting syndrome in gnotobiotic swine by coinfection with porcine circovirus 2 and porcine parvovirus.

One-day-old gnotobiotic piglets were inoculated intranasally with in vitro passaged porcine circovirus 1 (PCV-1), PCV-2, and porcine parvovirus (PPV) alone or in combination (PCV-1/PCV-2, PCV-1/PPV, and PCV-2/PPV). Piglets were evaluated for 1) the development of porcine postweaning multisystemic wasting syndrome (PMWS), 2) distribution of viral antigens by immunochemistry, and 3) viremia and the presence of viral DNA in nasal and ocular secretions and feces. All single agent-infected piglets and piglets infected with PCV-1/PCV-2 or PCV-1/PPV were clinically asymptomatic. They were transiently viremic and seroconverted to homologous virus(es). At termination of the study on postinfection day (PID) 35, microscopic lesions were restricted to focal inflammatory cell infiltrates in livers and myocardia. One piglet given PCV-1/PPV was PPV viremic for 2 weeks after infection and had lymphangiectasia of the spiral and descending colon associated with granulomatous inflammation. All four PCV-2/PPV-inoculated piglets developed PMWS, characterized by sudden onset of depression and anorexia, icterus, and submucosal edema. One piglet became moribund on PID 27, and the remaining three piglets were euthanatized between PID 27 and PID 30 because of severe disease. Lymph nodes were small and the livers were mottled. Disseminated angiocentric granulomatous inflammation was present in all tissues examined except the brain. Multiple lightly basophilic intracytoplasmic inclusion bodies were identified in macrophages and histiocytes. PCV-2 antigen was widely distributed within macrophages; PPV antigen was sparse. Hepatocellular necrosis and bile retention were prominent. PCV-2 DNA was identified in ocular, fecal, and nasal secretions. Terminal sera contained antibodies to PPV (4/4) and PCV-2 (3/ 4). Production of PMWS in gnotobiotic swine appears to require PCV-2 and additional infectious agents such as PPV for full disease expression in gnotobiotic piglets.

Animals↗

PubMed1996

The impact of pre-donated autologous blood and intra-operative isovolaemic haemodilution on the outcome of transfusion in patients undergoing radical retropubic prostatectomy.

OBJECTIVE: To assess the impact of pre-donated autologous blood and intra-operative isovolaemic haemodilution on the outcome of transfusions in patients undergoing radical retropubic prostatectomy. PATIENTS AND METHODS: The charts and transfusion records of 192 consecutive patients undergoing radical retropubic prostatectomy were reviewed retrospectively. RESULTS: Of 192 patients, 14% required homologous transfusions, the rate of which varied significantly depending upon blood availability (autologous, haemodilution or homologous) (P < 0.001): 66% of patients with only autologous blood available were transfused a mean of 1.96 units (range 1-6) of blood, of which 87% received autologous alone. 12% both autologous and homologous and 1% homologous blood only. Of the pre-donated autologous units, 44% were wasted. CONCLUSIONS: Both the pre-donation of autologous blood and intra-operative isovolaemic haemodilution lower the risk of homologous blood transfusion. It is recommended that patients pre-donate 2 units of autologous blood and undergo intra-operative isovolaemic haemodilution before radical prostatectomy.

Blood Transfusion, Autologous↗

PubMed2002

PCV2 replicase transcripts in infected porcine kidney (PK15) cells.

The Circoviridae family includes small viruses containing circular single strand DNA. There are two circoviruses described in pigs. Porcine Circovirus 2 (PCV2) has been linked to a disease termed Postweaning Multisystemic Wasting Syndrome (PMWS) whereas a close relative of this virus, termed PCV type 1 (PCV1) has been considered a non-pathogenic contaminant of the PK15 cell line. Rolling circle replication of small DNA viruses like circoviruses is mediated by a replicase (Rep) gene that is transcribed into different mRNAs by an alternative splicing mechanism. In PCV1, two transcripts Rep and Rep' implicated in DNA replication, have been identified from infected cells. These transcripts are the product of a single gene with Rep' having a different carboxyl end than Rep. Sequence comparison shows that there is a high degree of homology for the Rep gene in both viruses. In this article, we have identified three different transcripts by RT-PCR in PCV2 infected PK15 cells. Two of them have homology with their PCV1 counterparts and the third transcript, termed Rep", corresponds to another spliced version of the Rep gene. This transcript, unique to PCV2, encodes for a protein of 80 aminoacids in frame with the Rep sequence.

Amino Acid Sequence↗

PubMed2005

Prion biology relevant to bovine spongiform encephalopathy.

Bovine spongiform encephalopathy (BSE) and chronic wasting disease (CWD) of deer and elk are a threat to agriculture and natural resources, as well as a human health concern. Both diseases are transmissible spongiform encephalopathies (TSE), or prion diseases, caused by autocatalytic conversion of endogenously encoded prion protein (PrP) to an abnormal, neurotoxic conformation designated PrPsc. Most mammalian species are susceptible to TSE, which, despite a range of species-linked names, is caused by a single highly conserved protein, with no apparent normal function. In the simplest sense, TSE transmission can occur because PrPsc is resistant to both endogenous and environmental proteinases, although many details remain unclear. Questions about the transmission of TSE are central to practical issues such as livestock testing, access to international livestock markets, and wildlife management strategies, as well as intangible issues such as consumer confidence in the safety of the meat supply. The majority of BSE cases seem to have been transmitted by feed containing meat and bone meal from infected animals. In the United Kingdom, there was a dramatic decrease in BSE cases after neural tissue and, later, all ruminant tissues were banned from ruminant feed. However, probably because of heightened awareness and widespread testing, there is growing evidence that new variants of BSE are arising "spontaneously," suggesting ongoing surveillance will continue to find infected animals. Interspecies transmission is inefficient and depends on exposure, sequence homology, TSE donor strain, genetic polymorphism of the host, and architecture of the visceral nerves if exposure is by an oral route. Considering the low probability of interspecies transmission, the low efficiency of oral transmission, and the low prion levels in nonnervous tissues, consumption of conventional animal products represents minimal risk. However, detection of rare events is challenging, and TSE literature is characterized by subsequently unsupported claims of species barriers or absolute tissue safety. This review presents an overview of TSE and summarizes recent research on pathogenesis and transmission.

Animals↗

PubMed2000

Development of an immunoenzymatic assay for the detection of human antibodies against Trypanosoma cruzi calreticulin, an immunodominant antigen.

We have developed an indirect immunoenzymatic assay (ELISA) for the detection of human antibodies against calreticulin (formerly known as Tc45), a dimorphic Trypanosoma cruzi antigen, described in our laboratory. PVC microtitration plates were sensitized with the monoclonal anti-calreticulin antibody (MoAb) and reacted with calreticulin present in a partially purified preparation. The presence of anti-T. cruzi calreticulin IgG in sera from infected individuals was tested. The data generated with this assay were validated by correlation, in a regression analysis, with those obtained by an indirect immunoradiometric assay (IRMA). From the 12 seropositive sera (as defined by a commercial test), eight came out positive and four negative in both assays. The 12 human sera were also analyzed in direct immunometric assays (ELISA and IRMA), where the solid phase was sensitized with a whole parasite extract. The direct ELISA and IRMA correlated positively (P<0.01). Further validation of this ELISA was achieved with an indirect immunofluorescense assay. The high degree of significance obtained when the indirect IRMA and ELISA systems were compared, indicated that the relatively small sample number used (12) was statistically satisfactory for the purposes of this investigation. Thus, the IRMA can be replaced by the ELISA, with advantages mainly derived from the cumbersome manipulation of radioactive wastes. The MoAb used as an antigen capture agent in the ELISA proposed here, recognizes a homologous protein in Trypanosoma rangeli, suggesting that individuals infected with this parasite might have crossreactive antibodies. However, the system retains its diagnostic interest, given the facts that the MoAb does not recognize a homologous protein in Leishmania mexicana, Leishmania donovani, or Crithidia fasciculata.

Animals↗

PubMed2003

The heme oxygenase system: its role in liver inflammation.

Heme Oxygenase is the rate-limiting enzyme in the degradation of heme into carbon monoxide (CO), iron and bilirubin. To date, three heme oxygenase isozymes have been identified: HO-1, HO-2 and HO-3. While HO-1 is structurally different from its counterparts, HO-2 and HO-3 are very similar (90% homology), with HO-3 being a poor heme catalyst. Of the three isozymes, HO-1 is believed to be the only inducible form. Constitutively expressed HO-2 has been identified in several organs including kidney and vascular smooth muscle, with the most abundant sources (and activity) being in the liver, brain, spleen and testes. Within the normal liver, HO-2 is constitutively expressed within hepatocytes, Kupffer cells, endothelial cells and Ito cells. Until recently, products of the HO reaction were regarded as potentially toxic waste destined only for excretion. However, this view is changing as evidence suggests that HO activity plays an important protective role against cellular stress during inflammatory diseases. Biliverdin is reduced to bilirubin, which has been shown to possess potent antioxidative properties. CO, which is produced in equimolar concentrations to biliverdin and ferrous iron during heme oxidation by HO, may function as a second messenger stimulating soluble guanylate cyclase (sGC) and regulating vascular tone in combination with the free radical gas NO. CO may also possess anti-inflammatory properties such as the capacity to inhibit platelet aggregation, or the expression of pro-inflammatory cytokines. Recently, it has been shown that CO regulates bile formation and bile flow. We review the functional role of HO in liver and the potential application of HO-1 in therapeutic approaches to the treatment of inflammation.

Animals↗

PubMed2004

What have we learnt about the regulation of phosphate metabolism?

PURPOSE OF REVIEW: The search for hormones which specifically regulate phosphate metabolism has fuelled recent tantalizing studies. These studies have been motivated by diseases involving renal phosphate wasting, including tumor-induced osteomalacia, X-linked hypophosphatemic rickets, and autosomal dominant hypophosphatemia. This review focuses on likely candidate 'phosphatonins' and their possible physiological significance. RECENT FINDINGS: Candidate phosphatonins include fibroblast growth factor 23, matrix extracellular phosphoglycoprotein, stanniocalcin, and Frizzled-related protein 4. Fibroblast growth factor 23 has emerged as the prime candidate explaining pathophysiology of these diseases. FGF-23 is expressed in most tumors in tumor-induced osteomalacia. Serum fibroblast growth factor 23 is increased in most patients with X-linked hypophosphatemic rickets and tumor-induced osteomalacia. Injection of recombinant fibroblast growth factor 23 induces phosphaturia, hypophosphatemia, and suppression of 1,25-dihydroxyvitamin D in animals. Many unanswered questions remain, including the relationship between PHEX (phosphate-regulating gene with homologies to endopeptidases on the X chromosome) mutations and elevated fibroblast growth factor 23. It is also not clear whether these candidate phosphatonins play a role in phosphate or vitamin D metabolism in healthy humans, or that this role is endocrine. The most compelling evidence derives from the fibroblast growth factor 23-knockout mouse which shows hyperphosphatemia and increased serum 1,25-dihydroxyvitamin D. A physiologically relevant phosphatonin should explain renal adaptation to variable dietary phosphate intake. The tissue source and determinants of serum fibroblast growth factor 23 are unknown. SUMMARY: Pathophysiological and animal studies serve as a logical foundation on which to base further questions of human physiology. The definition of what is or is not a phosphatonin may need to be refined. There is a need to return to 'old-fashioned' human physiology studies to place recent findings in perspective.

Animals↗

PubMed2001

Mycobacterium immunogenum sp. nov., a novel species related to Mycobacterium abscessus and associated with clinical disease, pseudo-outbreaks and contaminated metalworking fluids: an international cooperative study on mycobacterial taxonomy.

PCR-restriction enzyme pattern analysis of a 439 bp hsp65 gene segment identified 113 unique isolates among non-pigmented rapidly growing mycobacteria (RGM) from clinical and environmental sources that failed to match currently recognized species patterns. This group represented 40% of isolates recovered from bronchoscope contamination pseudo-outbreaks, 0% of disease-associated nosocomial outbreaks and 4% of routine clinical isolates of the Mycobacterium abscessus/Mycobacterium chelonae group submitted to the Mycobacteria/Nocardia laboratory for identification. It is grouped within the Mycobacterium fortuitum complex, with growth in less than 7 d, absence of pigmentation, positive 3-d arylsulfatase reaction and growth on MacConkey agar without crystal violet. It exhibited overlapping biochemical, antimicrobial susceptibility and HPLC characteristics of M. abscessus and M. chelonae. By 16S rRNA gene sequencing, these isolates comprised a homogeneous group with a unique hypervariable region A sequence and differed by 8 and 10 bp, respectively, from M. abscessus and M. chelonae. Surprisingly, this taxon contained two copies of the ribosomal operon, compared with single copies in the two related species. By DNA-DNA hybridization, this new group exhibited <30% homology with recognized RGM species. The name Mycobacterium immunogenum sp. nov. is proposed for this new taxon.

Bacterial Proteins↗

PubMed1979

Results of renal transplantation using pediatric cadaver donors.

In order to determine the results of transplantation using pediatric cadaver donors, a retrospective analysis of a series of 502 renal transplant recipients was carried out. Methods of procurement, preservation, recipient selection, and immunosuppressive regimen were similar for all patients. Sixty-five recipients were approximately equally divided into three groups whose donors were younger than 5 years of age, 6 to 10 years old, and 11 to 15 years. These three groups then were compared with each other and to a randomly selected representative group of recipients whose donors were adults (16 years or older) for the following parameters: actuarial graft and patient survival, causes of graft failure and patient death, level of serum creatinine in currently functioning grafts, and recipient age. There were no statistically significant differences between groups for any parameter except that the mean age of recipients was approximately 16 years for the donors up to 5 years of age and was between 31 and 36 years for the other donor age groups (P = 0.01). These results support the contention that brain-dead pediatric patients of any age should be considered to be potential cadaveric kidney donors. Exclusion of these patients is very wasteful and also is unnecessary since results of transplantation equal to those obtained with adult donors can be expected. Technical graft failures should not be more frequent than with adult kidneys, and there is no need to modify the basic surgical technique for small kidneys in order to achieve this.

Adolescent↗

PubMed1987

Bone marrow transfers in X-irradiated mice congenic at the lpr locus: some paradoxical effects.

MRL/l mice, which are homozygous at the lpr locus, can be inhibited in lpr phenotype expression (lymphadenopathy, accelerated death) by a transfer of MRL/n bone marrow cells following X-irradiation of the recipients (MRL/n bone marrow----X-irradiated MRL/l chimeras). Female MRL/l bone marrow----X-irradiated MRL/l chimeras express the lpr phenotype with a delay corresponding to the age at the time of cell transfer. However, the equivalent male chimeras resemble MRL/n bone marrow----X-irradiated MRL/l chimeras. When the reverse MRL/l bone marrow----X-irradiated MRL/n chimeras are constructed, one finds that whichever the sex is, the chimeras undergo a wasting disease looking like a graft-versus-host disease, with particularly a marked atrophy of the spleen. A similar GVH like disease is observed with C57Bl/6 lpr bone marrow----X-irradiated C57Bl/6 normal mice. These animals survive at least 5 months but manifest a spleen aplasia. When reconstituted with MRL/n bone marrow, MRL/l recipients develop higher levels of antinuclear and anti-ds/ss DNA antibodies than MRL/n recipients. This suggests that the 'lpr environment' of the host may have an influence on the development of B cell hyperactivity.

Animals↗

PubMed2001

An agrin minigene rescues dystrophic symptoms in a mouse model for congenital muscular dystrophy.

Congenital muscular dystrophy is a heterogeneous and severe, progressive muscle-wasting disease that frequently leads to death in early childhood. Most cases of congenital muscular dystrophy are caused by mutations in LAMA2, the gene encoding the alpha2 chain of the main laminin isoforms expressed by muscle fibres. Muscle fibre deterioration in this disease is thought to be caused by the failure to form the primary laminin scaffold, which is necessary for basement membrane structure, and the missing interaction between muscle basement membrane and the dystrophin-glycoprotein complex (DGC) or the integrins. With the aim to restore muscle function in a mouse model for this disease, we have designed a minigene of agrin, a protein known for its role in the formation of the neuromuscular junction. Here we show that this mini-agrin-which binds to basement membrane and to alpha-dystroglycan, a member of the DGC-amends muscle pathology by a mechanism that includes agrin-mediated stabilization of alpha-dystroglycan and the laminin alpha5 chain. Our data provides in vivo evidence that a non-homologous protein in combination with rational protein design can be used to devise therapeutic tools that may restore muscle function in human muscular dystrophies.

Agrin↗

PubMed1997

Skeletal and cardiac myopathies in mice lacking utrophin and dystrophin: a model for Duchenne muscular dystrophy.

Dystrophin is a cytoskeletal protein of muscle fibers; its loss in humans leads to Duchenne muscular dystrophy, an inevitably fatal wasting of skeletal and cardiac muscle. mdx mice also lack dystrophin, but are only mildly dystrophic. Utrophin, a homolog of dystrophin, is confined to the postsynaptic membrane at skeletal neuromuscular junctions and has been implicated in synaptic development. However, mice lacking utrophin show only subtle neuromuscular defects. Here, we asked whether the mild phenotypes of the two single mutants reflect compensation between the two proteins. Synaptic development was qualitatively normal in double mutants, but dystrophy was severe and closely resembled that seen in Duchenne. Thus, utrophin attenuates the effects of dystrophin deficiency, and the double mutant may provide a useful model for studies of pathogenesis and therapy.

Animals↗

PubMed1987

Physiological responses to cachectin.

Mammals infected with parasitic, bacterial or viral organisms or bearing tumours characteristically display a catabolic state and weight loss which can advance to cachexia (or wasting), shock and death. Although the phenomenon is commonly observed in many parasitic diseases its mechanism is not understood. We have identified and isolated a macrophage protein, cachectin, as the molecule that may be responsible for cachexia and shock. Cachectin is produced by macrophages in response to endotoxin or a number of other bacterial or protozoal products. The released cachectin acts as a hormone, binding to specific high affinity receptors and eliciting biological responses. In the adipocyte anabolic enzymes such as lipoprotein lipase are suppressed through the selective inhibition of mRNA production. An intriguing aspect of cachectin is its pivotal role in the pathogenesis of endotoxin-induced shock. Cachectin causes fever and anorexia and can induce lethal shock and tissue injury in experimental animals. During its chemical characterization cachectin was shown to be identical to tumour necrosis factor (TNF), a macrophage protein that kills tumour cells. This finding emphasizes the extensive range of effects associated with this protein. Cachectin has many properties in common with interleukin 1 but binds to a different receptor and lacks structural homology. Presumably, low levels of cachectin help the host in its battle to remove invasive pathogens, but extensive production of cachectin can lead to shock and catabolic stress hormone responses. These findings have added a new dimension to the biological properties of cachectin, its production, and its role in cachexia and shock.

Animals↗

PubMed2001

Drosophila homolog of the myotonic dystrophy-associated gene, SIX5, is required for muscle and gonad development.

SIX5 belongs to a family of highly conserved homeodomain transcription factors implicated in development and disease. The mammalian SIX5/SIX4 gene pair is likely to be involved in the development of mesodermal structures. Moreover, a variety of data have implicated human SIX5 dysfunction as a contributor to myotonic dystrophy type 1 (DM1), a condition characterized by a number of pathologies including muscle defects and testicular atrophy. However, this link remains controversial. Here, we investigate the Drosophila gene, D-Six4, which is the closest homolog to SIX5 of the three Drosophila Six family members. We show by mutant analysis that D-Six4 is required for the normal development of muscle and the mesodermal component of the gonad. Moreover, adult males with defective D-Six4 genes exhibit testicular reduction. We propose that D-Six4 directly or indirectly regulates genes involved in the cell recognition events required for myoblast fusion and the germline:soma interaction. While the exact phenotypic relationship between D-Six4 and SIX4/5 remains to be elucidated, the defects in D-Six4 mutant flies suggest that human SIX5 should be more strongly considered as being responsible for the muscle wasting and testicular atrophy phenotypes in DM1.

Animals↗

PubMed1974

Immunological tolerance. Dissociation between in vivo and in vitro reactivity in parabiosed mice.

Although most mouse strain combinations succumb to a lethal wasting disease when parabiosed across a strong histocompatibility (H-2) barrier, a high proportion of DBA mice parabiosed to DBA/C3H F(1) hybrids survive and appear healthy. DBA mice accept C3H skin grafts following parabiosis, and may therefore be considered operationally tolerant of C3H antigens. Nonetheless, spleen cells from long-term DBA and F(1) parabionts give normal and enhanced responses, respectively, to C3H antigens in mixed lymphocyte culture (MLC). This indicates that the tolerance mechanism can distinguish between MLC recognition reactivity and in vivo effector reactivity, and that the former can therefore exist in the absence of the latter.

Animals↗

PubMed1976

Reconstitution of B and T lymphocyte function in severe combined immunodeficiency disease after transplantation with thymic epithelium.

A patient with severe combined immunodeficiency has been given a transplant of thymic epithelium obtained from short-term culture of normal human thymus. 4 wk after transplantation immunoglobulin was detected and the patient now has normal levels of the three main classes. Functional antibodies of four specificities have been detected. An increase in reactivity to allogeneic cells and phytohaemagglutinin has been observed, with an increase in E rosettes; a positive delayed skin test to candida antigen is now present. The patient has shown reversal of wasting and has been free of infection for 7 months since receiving the transplant. It appears that under certain circumstances thymic epithelium reconstitutes both T and B cell functions.

B-Lymphocytes↗